Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case is reported of a 66-year old man who developed Streptococcus bovis endocarditis on a fairly loose aortic stenosis and who also presented with alcoholic cirrhosis complicated by an ultimately lethal hepatoma. On this occasion, comments are made on the following points: -Str. bovis is increasingly responsible for bacterial endocarditis. This micro-organism is now rapidly and reliably identified. -Str. bovis endocarditis has some clinical features of its own. -Patients in whom the usual portals of entry of bacterial infection (i.e. benign or malignant tumours of the colon or rectum) cannot be identified should be investigated systematically for hepatic cirrhosis. -Drug sterilization of the gut is useful to prevent bacteremia of intestinal origin in cirrhotic patients.
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PMID:[Infectious endocarditis caused by Streptococcus bovis and alcoholic cirrhosis complicated by hepatoma]. 282 37

Natural killer (NK) activities of peripheral blood lymphocytes (PBL) in 50 patients with non-alcoholic liver cirrhosis (LC) were prospectively studied in order to clarify the relation between the development of hepatocellular carcinoma (HCC) and impaired NK activities. Patients were divided into two groups according to their NK activities at the beginning of the study, namely, Group A with normal NK activity (n = 21) and Group B with decreased NK activity (n = 29). NK activities were serially determined in each patient for up to 40 months. During the observation period, the occurrence of HCC was identified in 12 patients (four to 36 months). Of the patients who developed HCCs, two belonged to Group A (9.5%) and 10 belonged to Group B (34.5%). These results suggest decreased NK activity in LC patients to be one of the critical factors increasing their risk of developing HCC, and serial determinations of NK activities to be important in predicting the occurrence of HCCs in following the clinical course of LC patients.
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PMID:Relationship between natural killer activity and development of hepatocellular carcinoma in patients with cirrhosis of the liver. 282 47

Hepatocellular carcinoma tissues from HBsAg-negative patients with chronic alcoholic liver disease were investigated for the presence of hepatitis B virus DNA. Southern blot analyses of DNA extracted from the hepatocellular carcinomas were negative for hepatitis B virus DNA in all 17 patients examined, at a level of sensitivity of less than 0.01 genome equivalent per cell. Similarly, in liver tissues from another 30 patients with alcoholic cirrhosis without hepatocellular carcinoma, no hepatitis B virus DNA was detectable. We conclude that in our patients there is no molecular evidence for a contribution of hepatitis B virus infection to the development of hepatocellular carcinoma in alcoholic liver disease.
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PMID:Hepatocellular carcinoma in alcoholic liver disease: no evidence for a pathogenetic role of hepatitis B virus infection. 283 3

To investigate the possible role of sex-hormone imbalance in hepatocellular carcinogenesis in male alcoholic cirrhotic patients, we determined plasma levels of testosterone (T), dihydrotestosterone (DHT), androstenedione (A), dehydroepiandrosterone (DHA), estrone (E1), estradiol (E2), and sex-hormone-binding globulin (SHBG) in 15 men with alcoholic cirrhosis alone and in 15 similar men with alcoholic cirrhosis and hepatocellular carcinoma (HCC). The groups were matched for age and severity of liver disease using Child-Pugh scoring. Patients of both groups had evidence of hypogonadism with a decrease in plasma T levels (P less than 0.02) and of hyperestrogenemia with an increase in E1 (P less than 0.001), E2 (P less than 0.01), and SHBG (P less than 0.01) plasma levels compared with ten healthy age-matched controls. Cirrhotic patients with HCC had significantly lower plasma concentrations of T (P less than 0.02), DHT (P less than 0.01), and DHA (P less than 0.001) than patients with cirrhosis alone. However, the plasma concentrations of A, E1, E2, and SHBG did not significantly differ between these two groups. These results suggest a possible alteration of the estrogen-to-androgen ratio during carcinogenesis of the cirrhotic liver. This is shown by a greater reduction of circulating androgens and a similar elevation of estrogens in the group of cirrhotics with HCC.
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PMID:Sex hormone imbalance in male alcoholic cirrhotic patients with and without hepatocellular carcinoma. 284 Jan 90

From October 1982 to June 1985 158 hospitalized patients in the National Hospital of Niamey, Republic of Niger, were selected whenever one of the following signs was found: hepatomegaly, jaundice, ascites, oesophageal varices, abdominal venous pattern, or splenomegaly. Investigations included hepatic echography (158/158), needle liver biopsy (68/158), radioimmunoassays for serum hepatitis B surface antigen (HBsAg; 158/158), anti-HBs (152/158), anti-HBc (129/158) and anti-delta antibody (anti-HD; 158/158). 112 patients with liver diseases comprised 28 with chronic hepatitis, 55 with non-alcoholic hepatic cirrhosis, and 29 with hepatocellular carcinoma (HCC). 46 patients with other diagnoses were used as controls. 71/112 liver disease patients were positive for HBsAg in serum compared with 1/46 controls (P less than 10(-9)). Prevalences of delta superinfection in patients with serum HBsAg (+) and anti-HD (+) were 45/112 (40.2%) in liver disease patients versus 1/46 (2.2%) in controls (P less than 10(-9)). Delta superinfection was very frequent in chronic hepatitis (8/28), non-alcoholic cirrhosis (24/55) and HCC (14/29). In chronic hepatitis, delta superinfection was more frequent in the chronic active form than in the chronic persistent type (not significant). Cirrhosis patients with delta superinfection were younger (10 years in males, 11 years in females) than those without (P less than 0.05).
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PMID:Delta superinfection in patients with chronic hepatitis, liver cirrhosis and hepatocellular carcinoma in a Sahelian area. Study of 112 cases versus 46 controls. 284 9

Fourteen normal controls, eleven patients with non-alcoholic cirrhosis, twenty-nine with hepatocellular carcinoma (HCC) and six with HCC and hypoglycemia were studied. The tests performed include iv glucose tolerance test (25 g) and glucagon challenge test (2 mg). In cirrhosis, glucose intolerance and insulin resistance were demonstrated. The fasting hyperinsulinemia in cirrhosis is the result of decreased degradation as shown by the normal fasting C-peptide. The increased insulin responses to glucose, despite a normal C-peptide response, further supports the importance of impaired degradation in the pathogenesis of hyperinsulinemia after challenge. Despite a strong etiological association between cirrhosis and HCC, patients with HCC do not have significant hyperinsulinemia or glucose intolerance. This provides metabolic evidence to support the clinico-pathological observation that HCC occurred when cirrhosis was not advanced or in a precirrhotic stage. In HCC patients with clinically overt hypoglycemia, the fasting glucose, insulin and C-peptide were very low. The C-peptide responses to glucose and glucagon challenges were suppressed despite pharmacologic stimulation. This can be explained by the suppression of insulin secretion by a circulating substance secreted by hepatoma. The results support the pathogenetic importance of insulin-like activities recently detected in HCC patients with hypoglycemia.
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PMID:C-peptide in non-alcoholic cirrhosis and hepatocellular carcinoma. 284 76

A patient with alcoholic liver cirrhosis, diabetes mellitus and porphyria cutanea tarda (PCT) is described, who subsequently died of hepatocellular carcinoma. The literature relating PCT to the incidence of primary hepatoma is reviewed, and the mechanisms underlying this possible association are discussed.
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PMID:Is porphyria cutanea tarda a risk factor in the development of hepatocellular carcinoma? A case report and review of the literature. 298 17

The hypothesis that Mallory body formation by hepatocytes is a sign of preneoplasia was tested. This hypothesis was based on animal experiments but has not been tested in man. The authors studied the livers of 181 human autopsies in which hepatocellular carcinoma (HCC) was present and 82 cirrhotic livers from patients with alcoholism, HB viral infection, or cryptogenic cirrhosis. The frequency of Mallory bodies in nonneoplastic hepatocytes was 40% in the HCC-bearing livers with cirrhosis (LC). In HCC-bearing livers with pre-cirrhotic changes (PC), 25% showed Mallory body formation by nonneoplastic hepatocytes. In the cases of HCC, where there was no accompanying PC or LC, Mallory bodies were never found in the nonneoplastic hepatocytes. When the 82 cirrhotic livers without HCC and the 116 cirrhotic cases with HCC were combined, it was found that HCC was present in 70% of cirrhotic livers when the nonneoplastic liver cells contained Mallory bodies. When no Mallory bodies were found in the nonneoplastic liver cells, HCC was present in 53% of cases. The difference between the two groups was significant (P less than 0.05). The difference was significant for both HB viral hepatitis and cryptogenic cirrhosis but not for alcoholic cirrhosis. Likewise, when nonneoplastic hepatocytes formed Mallory bodies in cirrhotic livers, there was a statistically significant increase in the number of HCC cells that formed Mallory bodies (P less than 0.01). When nonneoplastic hepatocytes occurred in groups of Mallory body forming cells, the hepatocellular features were atypical and characteristic of dysplastic cells. The evidence indicates that when Mallory body formation was observed in HBsAg-positive and cryptogenic cirrhotic livers, they were associated with an increased frequency of HCC formation in man.
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PMID:Is mallory body formation a preneoplastic change? A study of 181 cases of liver bearing hepatocellular carcinoma and 82 cases of cirrhosis. 298 33

A rare autopsy case of combined liver cell and bile duct carcinoma (CLBC) occurring in a 51-year-old male with alcoholic liver cirrhosis is presented. Histologically, while the primary lesion was solely composed of well differentiated hepatocellular carcinoma (HCC), intrahepatic metastases consisted of a variable admixture of HCC and cholangiocarcinoma (CC) with excessive mucin production. Interestingly, the tumor cell cluster showing a trabecular growth pattern produced both bile and mucin, thus converting from HCC to mucinous CC. It is concluded that this liver malignancy is principally HCC with a marked tendency to transform into CC. The importance of the findings, especially the simultaneous production of bile and mucin within the same cell cluster, is emphasized in terms of the classification of CLBCs.
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PMID:Combined hepatocellular and mucinous carcinoma. 301 Jun 33

A patient is described with recurrent cholangitis and longstanding alcoholic cirrhosis. The cause of the cholangitis was found to be intraductal biliary tract invasion by hepatocellular carcinoma. A review of the literature suggests that this is an unusual manifestation of a common malignancy.
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PMID:Recurrent cholangitis caused by hepatocellular carcinoma. 301 Sep 27


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